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1. ⭐ 单胞多组 | Nat.Methods | 单细胞多组学检测DNA甲基化和组蛋白修饰重建表观基因组维持的动态过程

• ✍️ 作者：BioJournal Link
• 🏷️ 关键词：T细胞、单细胞、基因组、表观基因组、甲基化、组蛋白
• 🔗 查看原文

2. ⭐ 30+单细胞多组学通过解析DNA甲基化与组蛋白修饰，重构表观基因组维持的动态过程

• ✍️ 作者：作图丫
• 🏷️ 关键词：单细胞、基因组、表观基因组、甲基化、组蛋白
• 📝 描述：最近有小伙伴反映收不到推送，因为公众号改了推送算法，现在需要加星标，多点赞、点在看，才能准时收到推送哦。
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3. ⭐ NBE：嫁祸癌细胞！中国科学家发明通用型抗癌免疫疗法，让癌细胞表达乙肝病毒抗原，诱导特异性T细胞杀灭癌细胞

• ✍️ 作者：奇点肿瘤探秘
• 🏷️ 关键词：免疫、T细胞、B细胞、抗原
• 📝 描述：搞得癌细胞“一头雾水”。
• 🔗 查看原文

4. ⭐ 黄荷凤院士领衔！揭示代谢异常与表观遗传交叉调控多囊卵巢综合征新机制，PKM2介导的组蛋白乳酸化或是关键致病因素

• ✍️ 作者：转化医学网
• 🏷️ 关键词：代谢、代谢组、表观遗传、组蛋白
• 📝 描述：首次揭示丙酮酸激酶M2（PKM2）通过核易位促进组蛋白乳酸化修饰，重构三维基因组结构，从而激活PCOS关键致病基因的表达。
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5. ⭐ 单细胞+空转+代谢组，公开数据集找出亮点就能发1区12分

• ✍️ 作者：生信人
• 🏷️ 关键词：代谢、代谢组、单细胞
• 🔗 查看原文

6. ⭐ Cancer Cell重磅：肿瘤竟被自己人背刺！突变引爆免疫治疗

• ✍️ 作者：生信人
• 🏷️ 关键词：肿瘤、cancer、免疫
• 📝 描述：10月16日，Cancer Cell发表了德州大学MD安德森癌症中心Padmanee Sharma教授团队的重
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7. ⭐ 脚本更新–低精度（visium、stereo-seq bin > 50）的细胞邻域分析

• ✍️ 作者：单细胞空间交响乐
• 🏷️ 关键词：T细胞、B细胞、Visium
• 📝 描述：脚本更新–低精度（visium、stereo-seq bin > 50）的细胞邻域分析
• 🔗 查看原文

8. Dynamic-BW - 动态基因表达图谱【国家生物信息中心】

• ✍️ 作者：生信菜鸟团
• 🏷️ 关键词：生物信息、生信
• 📝 描述：Dynamic BodyMap 是一个涵盖时间序列 RNA 测序数据集中多个物种的数据库。
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9. 从零开始学习单细胞免疫组库（二）：学会深入解读结果文件！（文末赠书活动）

• ✍️ 作者：生信作曲家
• 🏷️ 关键词：免疫、单细胞
• 📝 描述：科学，循序渐进的单细胞免疫组库教程
• 🔗 查看原文

10. 塑造T细胞命运的免疫细胞

• ✍️ 作者：闲谈 Immunology
• 🏷️ 关键词：免疫、T细胞
• 🔗 查看原文

💡 该来源还有 21 条内容，详见 文末

详细内容（前10条）

1. ⭐ GSE298689 空间分辨单细胞分析揭示胶质母细胞瘤中具有抗肿瘤活性的蛋白激酶 Cδ 表达小胶质细胞 [空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、kinase、single-cell、spatial、spatially、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Reza Mirzaei ; Reid McNeil ; Charlotte D’Mello ; Britney Wong ; Susobhan Sarkar ; Frank Visser ; Candice Poon ; Pinaki Bose ; Wee YongSeries Type : OtherOrganism : Mus musculusThe glioblastoma (GBM) microenvironment contains resident immune cells with intrinsic anti-tumor potential, particularly microglia. Understanding the single-cell spatial heterogeneity and interactions between immune cells and brain tumor–initiating cells (BTICs) is essential for identifying therapeutic targets to reprogram immune responses and suppress BTIC growth. Using single-cell and spatial transcriptomics, we mapped immune cell populations in the GBM microenvironment and identified signaling networks mediating immune–cancer cell interactions. We discovered a previously unrecognized subset of microglia expressing protein kinase Cδ (PKCδ) with anti-tumor activity against BTICs. The presence of PKCδ-expressing microglia was validated in human GBM specimens. Enhancing PKCδ in microglia via adeno-associated virus or niacin increased phagocytosis of patient-derived BTICs in vitro and improved survival in GBM-bearing mice. Data from The Cancer Genome Atlas (TCGA) revealed that high PKCδ expression correlates with increased apoptosis, phagocytosis, and immune signaling pathways. These findings offer highlight PKCδ+ microglia as a promising therapeutic target in GBM.
• 🔗 查看原文

2. ⭐ GSE298688 空间分辨单细胞分析揭示胶质母细胞瘤中具有抗肿瘤活性的蛋白激酶 Cδ 表达小胶质细胞 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、kinase、single-cell、scRNA、spatially
• 📝 描述：Contributors : Reza Mirzaei ; Reid McNeil ; Charlotte D’Mello ; Britney Wong ; Susobhan Sarkar ; Frank Visser ; Candice Poon ; Pinaki Bose ; Wee YongSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe glioblastoma (GBM) microenvironment contains resident immune cells with intrinsic anti-tumor potential, particularly microglia. Understanding the single-cell spatial heterogeneity and interactions between immune cells and brain tumor–initiating cells (BTICs) is essential for identifying therapeutic targets to reprogram immune responses and suppress BTIC growth. Using single-cell and spatial transcriptomics, we mapped immune cell populations in the GBM microenvironment and identified signaling networks mediating immune–cancer cell interactions. We discovered a previously unrecognized subset of microglia expressing protein kinase Cδ (PKCδ) with anti-tumor activity against BTICs. The presence of PKCδ-expressing microglia was validated in human GBM specimens. Enhancing PKCδ in microglia via adeno-associated virus or niacin increased phagocytosis of patient-derived BTICs in vitro and improved survival in GBM-bearing mice. Data from The Cancer Genome Atlas (TCGA) revealed that high PKCδ expression correlates with increased apoptosis, phagocytosis, and immune signaling pathways. These findings offer highlight PKCδ+ microglia as a promising therapeutic target in GBM.
• 🔗 查看原文

3. ⭐ GSE285952：对接受过继性pmel-1 T细胞治疗或未治疗的小鼠（携带新抗原（B16KVP）或野生型（B16F10）肿瘤）的肿瘤和淋巴结进行Nanostring分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、lymph、T cell、regex:lymph(o|atic)?
• 📝 描述：Contributors : Amalia Rivera Reyes ; Hannah M KnochelmannSeries Type : Expression profiling by arrayOrganism : Mus musculusTwo separate experiments were performed. Experiment 1: Mice were subcutaneously injected with either B16F10 or B16KVP tumors. 6 days later, they were given 5Gy total body irradiation as a lymphdepletion regimen. Then the next day, 500,000 naïve pmel-1 CD8 T cells were injected via the tail vein into these mice. 5 days after adoptive cellular therapy, these mice were sacrified and the tumors and tumor draining lymph nodes harvested for Nanostring analysis. Experiment 2: Mice were subcutaneously injected with either B16F10 or B16KVP tumors. 6 days later, they were given 5Gy total body irradiation as a lymphdepletion regimen. Then the next day, mice were given no treatment or 500,000 naïve pmel-1 CD8 T cells were injected via the tail vein into these mice. 5 days after adoptive cellular therapy, these mice were sacrified and the tumors harvested for Nanostring analysis.
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4. ⭐ GSE307425 抗体靶向分泌蛋白 SCUBE3 通过抑制促肿瘤信号传导和诱导抗肿瘤免疫来抑制癌症生长和转移

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity、antibody
• 📝 描述：Contributors : Deepika Singh ; Benjamin C Onyeagucha ; Manjeet Rao ; Zhao Lai ; Yidong ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThrough a loss-of-function genomic screening approach, we identified Signal peptide CUB domain EGF-like 3 (SCUBE3) as a critical player for the survival and therapy resistance of cancer cells, particularly in triple negative breast cancer (TNBC). To further understand the mechanism by which SCUBE3 may support tumor growth and metastasis, we performed gene expression analysis on MDA-MB-231 cells stably silenced for SCUBE3. Pathway analysis reveled that Myc signaling, G2M checkpoint and DNA repair-associated genes were highly downregulated, while IFN gamma, inflammatory response and immunity-associated pathways were highly upregulated in SCUBE3-silenced TNBC cells.
• 🔗 查看原文

5. ⭐ GSE302247 二肽基肽酶 4 的恢复促进 KRAS-LKB1 突变型肺癌的抗肿瘤免疫

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity、KRAS
• 📝 描述：Contributors : Toshiyuki Tenma ; Ryohei Yoshida ; Hiraku Yanada ; Kiichi Nitanai ; Toshihiro Nagato ; Kyohei Oyama ; Nobunari Sasaki ; Mizuki Homme ; Chie Mori ; Takayuki Ohkuri ; Yusuke Ono ; Shoichiro Tange ; Yoshinori Minami ; Hiroya Kobayashi ; Yusuke Mizukami ; David A Barbie ; Shunsuke Kitajima ; Takaaki SasakiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensKRAS proto-oncogene, GTPase (KRAS)-liver kinase B1 (LKB1)-mutant (KL) non-small cell lung cancer (NSCLC), characterized by a profoundly immunosuppressive tumor microenvironment (TME), is highly resistant to immune checkpoint inhibitors (ICIs). Despite their high tumor mutation burden, KL tumors exhibit low programmed cell death ligand 1 (PD-L1) expression, reduced immune cell infiltration, and suppressed immune signaling pathways. Through systematic genomic analyses, we found that LKB1 loss suppresses dipeptidyl peptidase 4 (DPP4) expression and activity in KRAS-mutant lung cancer. Therefore, we evaluated the therapeutic potential of restoring DPP4 function to improve the immune response in KL lung cancer using patient-derived tumor samples and syngeneic mouse models. Restoration of DPP4 expression reprogrammed the TME and significantly increased immune-related gene signatures, including those involved in T cell migration and natural killer (NK) cell activation. Indeed, DPP4 restoration in three-dimensional microfluidic models enhanced NK cell chemotaxis and activity in targeting tumor spheroids. Furthermore, DPP4 restoration in syngeneic KL murine models synergized with anti-PD-1 therapy to achieve significant tumor regression. These findings suggest that LKB1 loss suppresses DPP4 expression, contributing to the immunosuppressive characteristics of the TME in KL-NSCLC cells, whereas, restoring DPP4 expression promotes NK cell recruitment, facilitates immune activation, and enhances the effects of anti-PD-1 therapy. These results highlight DPP4 as a key immune modulator and a promising therapeutic target, offering a novel strategy to overcome immune resistance and enhance immunotherapy outcomes in this challenging subset of lung cancer.
• 🔗 查看原文

6. ⭐ GSE309948 分泌激酶 FAM20C 触发脂肪细胞功能障碍，从而导致肥胖中的胰岛素抵抗和炎症

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、kinase、resistance
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusObesity is a major driver of type 2 diabetes (T2D) and related metabolic disorders, characterized by chronic inflammation and adipocyte dysfunction. However, the molecular triggers initiating these processes remain poorly understood. We identify FAM20C, a serine/threonine kinase, as an early obesity-induced mediator of adipocyte dysfunction. Fam20c expression is substantially upregulated in adipocytes in response to obesity, correlating with a proinflammatory transcriptional signature. Forced expression of Fam20c in adipocytes promotes robust upregulation of proinflammatory cytokines and induces insulin resistance that is dependent on its kinase activity. Conversely, deletion of adipocyte Fam20c after established obesity and hyperglycemia improves glucose tolerance, augments insulin sensitivity, and reduces visceral adiposity, without altering body weight. Phosphoproteomic studies reveal that FAM20C regulates phosphorylation of intracellular and secreted proteins, modulating pathways critical to inflammation, metabolism, and extracellular matrix remodeling. We identify FAM20C-dependent substrates, such as CNPY4, whose phosphorylation contributes to proinflammatory adipocyte signaling. Of translational relevance, we show that in humans visceral adipose FAM20C expression positively correlates with insulin resistance. Our findings establish FAM20C as an early regulator of obesity-induced adipocyte dysfunction and systemic metabolic impairment. Our studies provide proof of concept that inhibition of FAM20C may serve as a potential therapy for T2D by restoring adipocyte health.
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7. ⭐ GSE299929 研究表明，泛细胞周期蛋白依赖性激酶抑制剂是一种潜在的腺样囊性癌治疗方法，它能下调 MYB::NFIB 融合基因并​​诱导肿瘤消退。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、carcinoma、kinase
• 📝 描述：Contributors : Mattias K Andersson ; Junchi HuangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAdenoid cystic carcinoma (ACC) is a MYB-driven, aggressive glandular cancer with a poor long-term prognosis that is resistant to systemic therapies. Therefore, there is an urgent need to develop novel therapeutic strategies for these patients. An in vitro small-molecule inhibitor screen identified sensitivity of cultured ACC cells to pan-CDK inhibitors. We here used RNA-seq analysis to investigate the cell biological and molecular effects of treatment with the pan-CDK inhibitor dinaciclib in ACC cells from two different cases. Our results show that dinaciclib treatment led to a downregulation of genes involved in cell cycle progression, DNA replication, and DNA repair. Upregulated genes affected programmed cell death and included genes involved in proteolysis and autophagy. ACC MYB signature genes were significantly downregulated in dinaciclib-treated ACC cells, indicating that dinaciclib perturbs MYB-driven gene expression.
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8. ⭐ GSE306418 腹侧视网膜的进化重塑使四眼鱼 Anableps anableps 具备空中视觉 [空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Louise N. Perez ; Josane de Freitas Sousa ; Patricia SchneiderSeries Type : OtherOrganism : Anableps anablepsThe emergence of evolutionary novelties remains a central challenge in biology, particularly forcomplex organs such as the vertebrate eye. While visual systems have repeatedly undergonedegeneration or loss, examples of innovation are rare and poorly understood. Mechanistic insight intosuch gains requires tractable systems in which novel visual functions have evolved. Here we leverage thefour-eyed fish Anableps anableps to uncover the cellular and molecular basis of adaptation tosimultaneous aerial and aquatic light. Combining single-nucleus and spatial transcriptomics, we show thatthe Anableps ventral retina has been developmentally and functionally reconfigured for aerial vision. Infully aquatic teleosts such as zebrafish, ventral photoreceptors are tuned to red-shifted, downwelling light.In contrast, we show that Anableps exhibits an expanded and diversified ventral cone populationencompassing ultraviolet-, blue-, green-, and red-sensitive types, enabling broad-spectrum, high-intensityvision from above water. To estimate Anableps opsin spectral properties, we employed OPTICS, amachine-learning model of opsin spectral tuning, which predicts that the ventrally expressed opn1mw2opsin is red-shifted relative to typical green-sensitive pigments. Analysis of dorsal-ventral patterningmarkers reveals an overrepresentation of ventral retinal cell types. Consistent with this, comparativespatial transcriptomic profiling of developing and adult Anableps and the killifish (Fundulus heteroclitus)indicates a dorsal displacement of the dorsal-ventral boundary in Anableps, resulting in a proportionallylarger ventral retinal domain. Collectively, our results reveal that Anableps achieved its unique dual visualcapacity by developmentally expanding and functionally reprogramming the ventral retina for aerial lightdetection, an evolutionary innovation that redefines how retinal domains can adapt to radically differentvisual environments.
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9. ⭐ GSE305510 整合网络药理学、转录组学和单细胞测序技术探讨柔肝克力缓解肝硬化的作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell、transcriptomics
• 📝 描述：Contributors : Chengbo Jin ; Tianle Ma ; Yiheng Zhang ; Xujing Gu ; Tong Zhu ; Xinyu Wu ; Xin Ding ; Suzhou Huang ; Yulan Wang ; Zhipeng Chen ; Huihua Fang ; Li WuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackground: The progression of liver cirrhosis leads to severe complications, significantly threatening the survival and prognosis of patients. Rou gan ke li (Rgkl), a herbal formula derived from classical prescriptions, has used clinically over two decades and has good efficacy. However, its molecular mechanisms and active components remain undefined. Purpose: Exploring the molecular mechanisms of Rgkl in alleviating liver cirrhosis. Methods: CCl4-induced liver cirrhosis mice models were established. Liver stiffness and intrahepatic blood flow velocity were assessed using imaging. Serum ALT, AST, HA, and histopathology were analyzed. Hepatic stellate cells (HSCs) activation, liver sinusoidal endothelial cells (LSECs) fenestration, and angiogenesis were evaluated using immunohistochemistry and scanning electron microscopy. UPLC-Q-TOF-MS/MS and network pharmacology identified active components. Transcriptomics and single-cell sequencing identified key targets and pathways, validated via WB, immunofluorescence, and molecular docking. Results: Rgkl significantly reduced Liver stiffness and collagen deposition while increasing intrahepatic blood flow velocity in cirrhotic mice. Serum ALT, AST, and HA were markedly decreased. Rgkl inhibited α-SMA expression in HSC and downregulated pathological angiogenesis by reducing VEGF and CD34 expression. Additionally, Rgkl enhanced eNOS expression and preserved sinusoidal fenestration in LSEC. Furthermore, Rgkl ameliorated liver cirrhosis by modulating LSEC metabolic functions via the CD36/PPAR/CPT-1 pathway and suppressing HSC activation through the RhoA/ROCK/YAP and PI3K/AKT/NF-κB pathways. Eighteen active components, such as Levistilide A and Quercetin, were strongly correlated with the amelioration of liver cirrhosis. Conclusions: Rgkl significantly attenuated hepatic injury and fibrosis. Mechanistically, Rgkl modulated LSEC lipid metabolism and phenotypic regulation, and suppressed HSC contraction and activation. Key active components contributing to these effects included Paeonilactone C, Levistilide A, and Quercetin.
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10. ⭐ GSE288271 内源性逆转录病毒通过 RIG-I 通路促进系统性红斑狼疮中异常的 T 细胞分化 [全转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：T cell、transcriptomics、pathway
• 📝 描述：Contributors : Xiaoli Min ; Yaqian Yu ; Zhi HuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe dysregulated differentiation of T lymphocytes play an important role in systemic lupus erythematosus (SLE). However, the underlying mechanism remains unclear. Here, we screened and identified many overexpressed HERVs in CD4+ T cells from SLE patients by whole transcriptome resequencing and found that some HERVs formed dsRNAs to induce the activation of the RIG-I signaling pathway. And our findings reveal the roles and mechanism of HERVs and RIG-I in regulating the aberrant differentiation of T cells in SLE patients.
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1. ⭐ 由 BMP2/4-ACVR1 信号介导的肿瘤前巨噬细胞极化，在肿瘤起始过程中调控免疫抑制微环境

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤、免疫、免疫微环境、B细胞、巨噬细胞
• 📝 描述：Secret hovertext: 癌细胞能够通过制造免疫抑制性的“冷”肿瘤微环境（cTME）来规避免疫监测。更好地理解肿瘤形成初期 cTME 建立机制，有助于揭示更优的免疫治疗策略。为表征 cTME 形成的时间动态，我们在 EGFR 驱动肺腺癌（LUAD）起始阶段生成了单细胞 RNA 测序数据。TME 中的巨噬细胞经历了从抗肿瘤巨噬细胞向前肿瘤巨噬细胞的状态转变，这促成了 cTME 的形成。肿瘤细胞来源的 BMP2/4 诱导了前肿瘤巨噬细胞的极化，使用 ACVR1 抑制剂抑制 BMP2/4-ACVR1 轴，将 cTME 转化为“热”TME（hTME），从而有效抑制肿瘤生长。此外，EGFR 突变 LUAD 患者表现出与小鼠观察到的 cTME 相似特征，ACVR1 表达高与患者预后较差相关。总体而言，除了阐明前肿瘤巨噬细胞在 cTME 形成中的作用外，本研究还明确将 ACVR1 作为治疗 EGFR 突变肺癌的治疗策略。
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2. ⭐ 双特异性抗体与纳米技术：癌症免疫治疗中的战略联盟

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症、免疫、抗体
• 📝 描述：Secret hovertext: 双特异性抗体（bsAb）旨在识别两种不同的抗原或表位，使新一代癌症免疫疗法能够创新地发挥作用机制。尽管具有潜力，bsAb 治疗药物仍面临生物分布和药代动力学方面的诸多挑战，常常导致疗效与毒性平衡不佳。本综述从简要介绍 bsAbs 在癌症免疫治疗中的相关性开始，旨在批判性分析纳米技术与 bsAb 技术在提升治疗效率同时降低毒性方面的协同潜力。这种协同效应可以通过多种策略实现：（i）bsAbs 可能作为靶向配体，改善药物载荷纳米载体的生物分布;（ii）将治疗性 bsAbs 掺入纳米载体，可能轻松克服生物屏障，达到目标;以及（iii）bsAb 可以通过编码 mRNA 载体的纳米载体在体内生成。本综述探讨了这些新兴领域的挑战，并为该有前景领域的未来方向提供了见解。
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3. CRISPR-Cas9 筛查识别胰腺癌中对 KRAS 抑制的耐药机制

• ✍️ 作者：未知作者
• 🏷️ 关键词：耐药、KRAS
• 📝 描述：Secret hovertext: 针对各种 KRAS 突变的 KRAS 抑制剂（KRASi）已进入胰腺癌临床试验。尽管初步临床反应有希望，大多数患者因内在或后天性耐药性而复发。因此，联合治疗对于延长 KRAS 靶向疗法的疗效至关重要。为进一步确定 KRASi 耐药性的遗传机制，我们在 KRASG12D、KRASG12C、KRASG12R 和 KRASQ61H 突变 PDAC 细胞系中进行了 KRASi 锚定的 CRISPR-Cas9 功能丧失筛查，使用六个 KRASi，以识别调节对 KRAS 抑制敏感性的基因。通过联合靶向抑制剂与 KRASi，验证了包括 EGFR、CK2、p110α和 p110γ以及 YAP 在内的多个筛查结果。KRASQ61H 突变 PDAC 细胞系对 KRAS 的生存依赖性本质上低于其他 KRAS 突变亚型。此外，EGFR 抑制剂厄洛替尼与 RAS（ON）多选择性抑制剂 RMC-7977 在 KRASQ61H
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4. 线粒体转移挽救呼吸，支持嘧啶的生物合成和肿瘤进展

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤、线粒体
• 📝 描述：Secret hovertext: 线粒体 DNA（mtDNA）严重缺陷的癌细胞可以通过水平线粒体转移（HMT）导入线粒体以恢复呼吸。线粒体呼吸对于二氢食氧酸脱氢酶（DHODH）的活性至关重要，DHODH 是一种来自线粒体内膜的酶，催化新生嘧啶合成的第四步。本研究研究了嘧啶新生合成在驱动线粒体 DNA 缺乏（ρ0）细胞肿瘤生长中的作用。虽然在小鼠体内移植的ρ0 细胞容易获得线粒体 DNA，但在采用替代氧化酶（AOX）转染的细胞中，这一过程被延迟，AOX 结合了线粒体呼吸复合体 III 和 IV 的功能。ρ0 AOX 细胞具有糖解作用，但保持正常的 DHODH 活性和嘧啶的产生。在一组肿瘤细胞中 DHODH 的缺失完全阻断或延缓肿瘤生长。这些移植的ρ0 细胞迅速招募了先天免疫系统中促进肿瘤/稳定的细胞，包括肿瘤前 M2 巨噬细胞、中性粒细胞、嗜酸性粒细胞和间充质间质细胞（MSCs）。ρ0 细胞在移植后早期招募了 MSCs，这些
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5. 催化抑制 p300 优先针对 IRF4 致癌活性和多发性骨髓瘤肿瘤生长

• ✍️ 作者：未知作者
• 🏷️ 关键词：肿瘤
• 📝 描述：Secret hovertext: 致癌转录因子（TF）IRF4 是一种目前尚未被完全确定的普遍多发性骨髓瘤（MM）依赖性。通过转录调控网络（TRN）定位，一种无偏多组目标识别方法，我们鉴定出共激活剂赖氨酸乙酰转移酶（KAT）p300 作为关键的 IRF4 伙伴。通过定量相互作用组图谱验证了这一偏好关系，发现 IRF4 是 MM 特异性依赖最丰富的，且比其他转录因子如 IKZF1/IKZF3 与 p300 更为紧密复合。优化的 p300 赖氨酸乙酰转移酶（KAT）抑制剂使 IRF4 活性和 MM 增殖在体外和体内均得以抑制。p300/CBP KAT 抑制优先针对 MM 细胞而非正常细胞，特异性调节 MM 转录组，且 p300 KAT 抑制剂在较低水平下更完全抑制 IRF4 活性，相较于现有 p300/CBP 溴结构域抑制剂。此外，结合 p300/CBP KAT 抑制剂及治疗方法，结合针对 MM 转录的正交机制，产生了协同抗肿瘤效应。这些数据共同推动了
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6. GRPR 诱导的 FAM135A 表达促进前列腺癌的神经周浸润

• ✍️ 作者：未知作者
• 🏷️ 关键词：神经
• 📝 描述：Secret hovertext: 神经周围浸润（PNI）是前列腺癌（PCa）转移的独立不良预后标志物。胃泌素释放肽受体（GRPR）靶向影像和治疗已进入临床试验阶段，其在 PCa 神经周围侵袭中的作用尚不明确。在这里，我们发现了序列相似度 135 的家族成员 A（成员 A）༈FAM135A༉a 显性 PNI 驱动体，在 PCa 中被 GRPR 激活。首先，PNI-PCa 组织表现出更高的神经活性配体-受体相互作用活性，其中 FAM135A 是 PNI 组中最显著的标志。随后，体外实验使用 PCa 细胞共培养系统（包括 AR 阳性 LNCaP 和 AR 阴性 DU145/PC3）显示，消灭肿瘤恶性肿瘤和神经侵袭 FAM135A。此外，体内 PCa-坐骨神经侵袭小鼠模型显示 FAM135A 抑制能控制肿瘤生长并改善运动功能。有趣的是，FAM135A 细胞核富集，其核易位由蛋白质细胞质-核转运蛋白 RAN 介导。从机制上看，RNA-Seq
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详细内容（全部1条）

1. 亚马逊蝎毒液展现出对抗乳腺癌的惊人功效

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists are turning venom, radioisotopes, engineered proteins, and AI into powerful new tools against cancer. From Amazonian scorpions yielding molecules that kill breast cancer cells as effectively as chemotherapy, to improved fibrin sealants and custom-grown bioactive factors, researchers are pushing biotechnology into uncharted territory. Parallel teams are advancing radiotheranostics that diagnose and destroy tumors with precision, while others forge experimental vaccines that train the immune system using hybrid dendritic cells.
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• GSE308299 研究发现，在卵巢癌临床前模型中，JNK 敲低通过 NFATc1 增强 CAR-T 细胞的细胞毒性。
• GSE306569 球状体培养揭示了三阴性乳腺癌中癌症干细胞的富集和独特的化疗反应
• GSE306950 NK细胞活化失调和髓系-淋巴系失衡是COPD进展的基础：来自高维免疫分析和吸烟诱导的免疫重塑的启示
• GSE298464 单细胞 RNA 测序揭示溃疡性结肠炎患者对 TNF-α 抑制剂治疗的反应
• GSE297006 内源性逆转录病毒通过 RIG-I 通路促进系统性红斑狼疮中异常的 T 细胞分化 [SLE]
• GSE296556 内源性逆转录病毒通过 RIG-I 通路促进系统性红斑狼疮中异常的 T 细胞分化 [mouse_CD4]
• GSE296447 独特的空间组织调控口腔黏膜免疫
• GSE292853 Ribo-lite 是一种在低起始量下对接受 5+3 或载体治疗并喂食标准氨基酸 (AA) 或不含支链氨基酸 (BCAA) 饮食的小鼠 AML 细胞进行配对转录组 (RNA-seq) 和翻译组 (Ribo-seq) 分析的方法。[II]
• GSE288272 内源性逆转录病毒通过 RIG-I 通路促进系统性红斑狼疮中异常的 T 细胞分化 [幼稚]
• GSE283618 FSTL3 过表达是调控同基因小鼠卵巢肿瘤微环境的关键因素
• GSE280939 发现一种小尺寸咪唑-苯并吲哚配体，该配体可与 KRAS 启动子 G-四链体结合，抑制癌症生长并增强免疫调节作用
• GSE266202 EZH2 抑制引起的表观遗传变化增加高 AID 活性或 DNA 修复缺陷的 B 细胞中的易位 [RNA-Seq]
• GSE255082 高血压通过交感神经激活外周免疫系统促进海马炎症和认知障碍
• GSE231781 患者来源宫颈类器官的单细胞图谱揭示了衣原体感染期间上皮免疫异质性和细胞间相互作用
• GSE231775 患者来源宫颈类器官的单细胞图谱揭示了衣原体感染期间上皮免疫异质性和细胞间相互作用
• GSE231773 患者来源宫颈类器官的单细胞图谱揭示了衣原体感染期间上皮免疫异质性和细胞间相互作用
• GSE300915 骨巨噬细胞吞噬作用诱导的代谢转变驱动乳酸生成并调节炎症和破骨细胞生成
• GSE298405 利用 AAV9-ME CRISPR 文库在小鼠肺部炎症模型中筛选必需代谢介质
• GSE289642 非经典 PRC2 染色质关联揭示 EZHIP 在代际表观遗传记忆转变中的关键作用 [ChIP-Seq, Cut & Run]
• GSE289641 非经典 PRC2 染色质关联揭示 EZHIP 在代际表观遗传记忆转变中的关键作用 [RNA-Seq]
• GSE228743 HOXB13 通过与 SWI/SNF 复合物的相互作用改变前列腺癌中的染色质可及性 [ChIP-seq ]
• GSE228742 HOXB13 通过与 SWI/SNF 复合物的相互作用改变前列腺癌中的染色质可及性 [ATAC-seq ]
• GSE310403 果蝇 yki 肿瘤组织两种版本的 RNA 测序分析
• GSE310343 IL-22 来自肠内分泌细胞，通过微生物群促进斑马鱼早期肠道蠕动
• GSE309795 酪氨酸激酶抑制剂心脏毒性的多尺度分析揭示机械敏感离子通道 PIEZO1 具有心脏保护作用 [bulk RNA-seq]
• GSE297742 前列腺腺癌患者原发肿瘤活检样本的批量RNA测序
• GSE297652：M1期前列腺癌患者转移灶活检和外周血单核细胞的单细胞转录组谱
• GSE310316 Nox4抑制剂治疗可改善杜氏肌营养不良症小鼠模型的心脏功能
• GSE310057 对 RiboCancer 细胞系面板的翻译组和翻译动力学分析表明，白血病相关的 Rps15 突变通过密码子特异性 tRNA 适应缺陷重塑翻译。
• GSE251803 转录因子 PLT 和染色质调节因子 PRC2 和 JMJ703 形成核凝聚体，以维持控制水稻根分生组织细胞命运的二价结构域中的基因抑制 [RNA-Seq]
• GSE310346 EZH2 抑制引起的表观遗传改变增加高 AID 活性或 DNA 修复缺陷的 B 细胞中的易位 [MEC-1 细胞的 LAM-HTGTS ]
• GSE310332 EVT0185 对乙酰辅酶A代谢酶的抑制作用可损害肝星状细胞活化，并逆转小鼠模型中的MASH和纤维化[nanostring]
• GSE304764 母体补充蛋氨酸诱导绵羊卵母细胞和胚胎的表观遗传重塑
• GSE303874 河口海豚脑组织RNA测序
• GSE302875 AngII 加盐诱导的小鼠腹主动脉瘤的单细胞转录组学研究[28 天]
• GSE299152 成人和小鼠眼表糖萼的单细胞定位
• GSE298041 肺上皮损伤损害先天防御并重编程巨噬细胞功能，降低早期结核分枝杆菌清除率
• GSE297736 EZH2 抑制引起的表观遗传变化增加高 AID 活性或 DNA 修复缺陷的 B 细胞中的易位 [MEC-1 中的 HTGTS]
• GSE296068 低输入量转座酶可及染色质检测方法鉴定肝脏 1 组固有淋巴细胞的表观遗传特征
• GSE295455 体外金黄色葡萄球菌刺激绵羊乳腺上皮细胞的高通量转录组学分析
• GSE294437 HERV-K10 作为肝炎感染中免疫调节的介质
• GSE293984 连接纤毛、应激反应和蛋白质稳态异常，为 RPGRIP1 视网膜类器官的变异和治疗评估提供信息 [scRNA-seq]
• GSE293982 连接纤毛、应激反应和蛋白质稳态异常，为 RPGRIP1 视网膜类器官的变异和治疗评估提供信息 [RNA-Seq]
• GSE292171 用或不用 MLN4924 处理的巨噬细胞的 RNA 测序
• GSE290428 早期饥饿和 Hedgehog 相关信号激活 daf-18/PTEN 和 lin-35/Rb 下游的先天免疫，导致成年秀丽隐杆线虫发育病理
• GSE290063 番茄果实采后经UV-C照射后的转录组和表观遗传特征与果实品质的保持相关
• GSE286009 MFF 标志着多发性骨髓瘤的代谢脆弱性
• GSE284296 胶质瘤细胞系 LN229 和 U87 中糖RNA的分析
• GSE282762 表观基因组操作揭示了位点特异性染色质动态与基因表达之间的关系 [RNA-seq]
• GSE282761 表观基因组操作揭示了位点特异性染色质动态与基因表达之间的关系 [Hi-C]
• GSE282760 表观基因组操作揭示了位点特异性染色质动态与基因表达之间的关系 [ChIP-seq]
• GSE282486 有丝分裂期 Polo 样激酶 1 的批量 ATACseq 分析表明，有丝分裂期转录和染色体可及性得以维持
• GSE267993 ZNHIT3 调控翻译以确保小鼠植入前发育 [scRNA-Seq]
• GSE266298 EZH2抑制引起的表观遗传改变会增加AID活性高或DNA修复缺陷的B细胞的易位。
• GSE266270 EZH2 抑制引起的表观遗传变化增加高 AID 活性或 DNA 修复缺陷的 B 细胞中的易位 [GRO-seq]
• GSE266267 EZH2 抑制引起的表观遗传改变会增加 AID 活性高或 DNA 修复缺陷的 B 细胞的易位 [H3K27ac 的切割和标记]
• GSE266237 EZH2 抑制引起的表观遗传改变会增加高 AID 活性或 DNA 修复缺陷的 B 细胞中的易位 [LAM-HTGTS for CH12F3 cell]
• GSE266205 EZH2 抑制引起的表观遗传改变会增加高 AID 活性或 DNA 修复缺陷的 B 细胞中的易位 [H3K27me3 的切割和标记]
• GSE261167 细菌RNA通过秀丽隐杆线虫的组织间通讯促进蛋白质稳态
• GSE310263 mRNA N6-甲基腺苷 (m6A) 在高 L-2-羟基戊二酸肾癌中的生物学作用
• GSE309870 APOBEC3B 增强 PARP 抑制剂清除卵巢癌干细胞的疗效
• GSE300925 巨噬细胞中 Lyn 的表达促进 TLR 激活并以一种不依赖于亚型的方式限制增殖。
• GSE297645 小分子 ITK 和泛 TRK 激酶抑制剂 (PF-07245303) 用于特应性皮炎的潜在局部治疗
• GSE289282 非经典 PRC2 染色质关联揭示 EZHIP 在代际表观遗传记忆转换中的关键作用
• GSE273480 lncRNA CISTR-ACT 调控人和小鼠的细胞大小 [ChIP-seq]
• GSE273476 lncRNA CISTR-ACT 调控人和小鼠的细胞大小 [RNA-seq]
• GSE253048 第11天对照组、光子和质子照射组唾液腺类器官的单细胞测序分析
• GSE253034 RNA测序分析对照组、光子和质子照射组唾液腺类器官在照射后2天和6天的情况
• GSE252164 主动脉瓣反流微创手术后心脏重塑的转录组分析
• GSE310282 结肠上皮和固有层来源的 Treg 的 RNA 测序
• GSE310225 精细化的细胞活性表达特征为量化单细胞数据中的肿瘤内表型异质性提供了一个靶向框架
• GSE309878 神经发育障碍患者中表观遗传调控因子 PHF20 的纯合缺失
• GSE309861 KLF5 控制胰腺癌中与亚型无关的高相互作用增强子以调节细胞存活 [HiChIPseq]
• GSE309860 KLF5 控制胰腺癌中与亚型无关的高相互作用增强子以调节细胞存活 [ChIPseq]
• GSE299636 WDR5 重塑 NANOG 凝聚体以驱动转录程序并维持干细胞特性 [ChIP-seq]